4.6 Review

Immunobiology of spinal cord injuries and potential therapeutic approaches

Journal

MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 441, Issue 1-2, Pages 181-189

Publisher

SPRINGER
DOI: 10.1007/s11010-017-3184-9

Keywords

Spinal cord injury; Immunological impact; Therapy; Immune cells; Astrocytes; Macrophages; Neutrophils

Categories

Funding

  1. National Heart, Lung and Blood Institute, National Institutes of Health, USA [R01 HL116042, R01 HL112597, R01 HL120659]
  2. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL116042, R01HL112597, R01HL120659] Funding Source: NIH RePORTER

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The incidence of spinal cord injuries (SCI) is high every year. As the spinal cord is the highway that allows for the brain to control the rest of the body, spinal cord injuries greatly impact the quality of life of the patients. The SCI include the primary response consisting of the initial accident-induced damage and the secondary response that is characterized by damage due to inflammation and biological responses. Astrocytes are the first to act at the site of the injury, forming a glial scar and attracting immune cells. The immune system plays a role in cleaning out the debris caused by the injury, as well as preventing neurons to grow and heal. The secondary injury caused by the inflammatory response is the major target to combat SCI. This article critically reviews the key players in the inflammatory SCI response and potential therapies, specifically targeting astrocytes, neutrophils, and macrophages. These cells are both beneficial and detrimental following SCI, depending on the released molecules and the types of cells infiltrated to the site of injury. Indeed, depending on the subtype of macrophages, M1 or M2, beneficial or detrimental response could be incited. Therapeutic strategies to regulate and manipulate the immune cells via increasing or decreasing their recruitment to the site of injury could be developed together with upregulating and downregulating the release of certain chemicals from the infiltrated cells.

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